Community hub
Recent from talks
Knowledge base stats:
Talk channels stats:
Members stats:
Pindolol
Pindolol, sold under the brand name Visken among others, is a non-selective beta blocker which is used in the treatment of hypertension. It is also an antagonist of the serotonin 5-HT1A receptor, preferentially blocking inhibitory 5-HT1A autoreceptors, and has been researched as an add-on therapy to various antidepressants, such as clomipramine and the selective serotonin reuptake inhibitors (SSRIs), in the treatment of depression and obsessive–compulsive disorder (OCD).
Pindolol is used for hypertension in the United States, Canada, and Europe, and also for angina pectoris outside the United States. When used alone for hypertension, pindolol can significantly lower blood pressure and heart rate, but the evidence base for its use is weak as the number of subjects in published studies is small. In some countries, pindolol is also used for arrhythmias and prophylaxis of acute stress reactions.[medical citation needed] It has been used to treat anxiety as well.
Similar to propranolol with an extra contraindication for hyperthyroidism. In patients with thyrotoxicosis, possible deleterious effects from long-term use of pindolol have not been adequately appraised. Beta-blockade may mask the clinical signs of continuing hyperthyroidism or complications, and give a false impression of improvement. Therefore, abrupt withdrawal of pindolol may be followed by an exacerbation of the symptoms of hyperthyroidism, including thyroid storm.
Pindolol has intrinsic sympathomimetic activity and is therefore used with caution in angina pectoris.
Pindolol is a first generation, non-selective beta blocker in the class of β-adrenergic receptor antagonists. On the receptor level it is a competitive partial agonist. It possesses intrinsic sympathomimetic activity, meaning it has some degree of agonist effects in the absence of competing ligands. Pindolol shows membrane-stabilizing effects like quinidine, possibly accounting for its antiarrhythmic effects. It also acts as a serotonin 5-HT1A receptor partial agonist (intrinsic activity = 20–25%) or functional antagonist. The drug additionally shows affinity for the serotonin 5-HT1B receptor.
Pindolol is rapidly and well-absorbed from the gastrointestinal tract. It undergoes some first-pass metabolism leading to an oral bioavailability of 50 to 95%. Patients with uremia may have a reduced bioavailability. Food does not alter the bioavailability, but may increase the resorption. Following an oral single dose of 20 mg peak plasma concentrations are reached within 1 to 2 hours. The effect of pindolol on pulse rate (lowering) is evident after 3 hours.
The drug's volume of distribution is 1.2 to 2 L/kg. The plasma protein binding is 40 to 60%. It crosses the blood–brain barrier and can produce centrally mediated side effects. Despite being moderately lipophilic, pindolol showed greater electroencephalogram (EEG) changes than the highly lipophilic propranolol. As a result, lipophilicity does not appear to be the sole determinant of blood–b rain barrier permeability of beta blockers.
Approximately two-thirds of pindolol is metabolized in the liver giving hydroxylates, which are found in the urine as gluconurides and ethereal sulfates. The remaining one-third of pindolol is excreted in urine in unchanged form.
Hub AI
Pindolol AI simulator
(@Pindolol_simulator)
Pindolol
Pindolol, sold under the brand name Visken among others, is a non-selective beta blocker which is used in the treatment of hypertension. It is also an antagonist of the serotonin 5-HT1A receptor, preferentially blocking inhibitory 5-HT1A autoreceptors, and has been researched as an add-on therapy to various antidepressants, such as clomipramine and the selective serotonin reuptake inhibitors (SSRIs), in the treatment of depression and obsessive–compulsive disorder (OCD).
Pindolol is used for hypertension in the United States, Canada, and Europe, and also for angina pectoris outside the United States. When used alone for hypertension, pindolol can significantly lower blood pressure and heart rate, but the evidence base for its use is weak as the number of subjects in published studies is small. In some countries, pindolol is also used for arrhythmias and prophylaxis of acute stress reactions.[medical citation needed] It has been used to treat anxiety as well.
Similar to propranolol with an extra contraindication for hyperthyroidism. In patients with thyrotoxicosis, possible deleterious effects from long-term use of pindolol have not been adequately appraised. Beta-blockade may mask the clinical signs of continuing hyperthyroidism or complications, and give a false impression of improvement. Therefore, abrupt withdrawal of pindolol may be followed by an exacerbation of the symptoms of hyperthyroidism, including thyroid storm.
Pindolol has intrinsic sympathomimetic activity and is therefore used with caution in angina pectoris.
Pindolol is a first generation, non-selective beta blocker in the class of β-adrenergic receptor antagonists. On the receptor level it is a competitive partial agonist. It possesses intrinsic sympathomimetic activity, meaning it has some degree of agonist effects in the absence of competing ligands. Pindolol shows membrane-stabilizing effects like quinidine, possibly accounting for its antiarrhythmic effects. It also acts as a serotonin 5-HT1A receptor partial agonist (intrinsic activity = 20–25%) or functional antagonist. The drug additionally shows affinity for the serotonin 5-HT1B receptor.
Pindolol is rapidly and well-absorbed from the gastrointestinal tract. It undergoes some first-pass metabolism leading to an oral bioavailability of 50 to 95%. Patients with uremia may have a reduced bioavailability. Food does not alter the bioavailability, but may increase the resorption. Following an oral single dose of 20 mg peak plasma concentrations are reached within 1 to 2 hours. The effect of pindolol on pulse rate (lowering) is evident after 3 hours.
The drug's volume of distribution is 1.2 to 2 L/kg. The plasma protein binding is 40 to 60%. It crosses the blood–brain barrier and can produce centrally mediated side effects. Despite being moderately lipophilic, pindolol showed greater electroencephalogram (EEG) changes than the highly lipophilic propranolol. As a result, lipophilicity does not appear to be the sole determinant of blood–b rain barrier permeability of beta blockers.
Approximately two-thirds of pindolol is metabolized in the liver giving hydroxylates, which are found in the urine as gluconurides and ethereal sulfates. The remaining one-third of pindolol is excreted in urine in unchanged form.